Last updated: Wed, Jul 31, 2024
The expectation that a painful event is about to occur seems to increase sensitivity to it. The expectation of pain can be based on events that are not themselves painful.
Primate subjects were trained to press a button after a light was turned on. After pressing the button, the subject was subjected to painful heat. Activity in dorsal horn neurons of the subjects was recorded (see Organization of the Spinal Cord). Some of these neurons became more active either when the light went on or when the subject pressed the button, before the heat was turned on. Thus, pain sensitivity was changed by events that the subjects had learned to associate with imminent pain.
Experiments on human subjects have shown that they are more likely to interpret a stimulus as painful after they have received a cue that they are about to receive a painful stimulus.1
Physiologic evidence supports these findings and provides a mechanism for this phenomenon. Brain imaging studies show that areas of the limbic system (including the nucleus accumbens or NAc and the anterior cingulate cortex or ACC) and the brain stem (PAG/RVM areas) are activated by the learned cues before the painful stimulus occurs. This indicates that the sensitivity of the spinal cord to pain can be changed by these learned, non-pain cues.
This physiologic mechanism is part of a larger and more general system concerned with directing attention and action. The system can turn sensitivity to pain up or down depending on the situation, which results in the phenomenon that we call "pain modulation." Although being insensitive might be more pleasant in the short run, the system seems to err on the side of caution, choosing to emphasize knowledge of possible harm. In the context of behavior, the same system can turn down the pain to allow important activities (such as eating, micturition, etc.) to occur in the presence of painful sensory input. Experimenters have reported that more analgesia occurs when the food is more appetizing.2
The reviewer of these results stated that they raise the intriguing possibility that pain can be produced by a centrally originating drive of dorsal horn nociceptive neurons, without activation of primary afferent nociceptors.
3 So far as I can make out, this is merely speculation by the reviewer. (Is it another example of a researcher actively seeking evidence that pain may be illusory? What motivates this?) However, the effect of expecation in increasing perceived pain is well-established.
It seems to me most straightforward to see this as an adaptive attentional feature of the pain system. In normal biologic circumstances pain is important information.
What are the implications of the role of expectancy in pain perception?